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Periodontal Disease

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Abstract

Periodontitis (PD) is a widespread inflammatory disease of the oral cavity. A deregulated inflammatory reaction leads to gingival bleeding, pocket formation, destruction of the connective tissue attachment and alveolar bone with subsequent tooth loss. Lifestyle factors, in particular tobacco use and diabetes, determine disease susceptibility and contribute to the progression but PD is initiated by pathogenic microorganisms in the subgingival biofilm. The oral microbes are traditionally regarded as the principal cause of PD but the concept emerges that the host genotype shapes the antimicrobial response that promotes disease development rather than a single microbial composition. This highlights the importance of understanding the patients’ genomic differences as critical factors for the personal disease susceptibility. The current knowledge of the molecular genetic etiology of PD is limited to a few loci, most importantly ANRIL , CAMTA1/VAMP3, NPY, PLG and GLT6D1, which gave evidence of disease relevance by statistically significant associations and replication in large homogenous study populations. These genes are largely located in regulatory networks that integrate interactions of the metabolic and immune system and suggest pathogenic mechanisms of obesity-induced inflammation as a likely common pathogenic denominator of PD, offering substantial therapeutic promise. Yet, the identified risk alleles only explain a small proportion of the heritability, which is in large parts due to statistical limitations of the available clinical analysis populations. Where the missing heritability lays is currently unknown. Prerequisite for the identification of the unknown risk alleles, with all expected translational effects on diagnosis and therapy, is the creation of large research consortia that enable the collection of sufficiently powered samples.

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Schäfer, A. (2015). Periodontal Disease. In: Sonis, DMD, DMSc, S. (eds) Genomics, Personalized Medicine and Oral Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-17942-1_7

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